OLR1 Is a Pan-Cancer Prognostic and Immunotherapeutic Predictor Associated with EMT and Cuproptosis in HNSCC.

Metabolism plays a critical role in cancer. has been implicated in cardiovascular and metabolic disorders, while its association with tumorigenesis and tumor immunity remains poorly defined in the literature. We conducted comprehensive pan-cancer analyses based on the TCGA database to examine expression and its prognostic implications. Correlations between expression level and tumor immunity and immunotherapy were investigated by immune infiltration, enrichment, and TIDE analysis methods. Immunohistochemistry detected expression in HNSCC. We used the GSEA method to explore the potential signaling pathways in which is involved, and a correlation analysis to investigate the relationships between and epithelial-mesenchymal transition (EMT) and cuproptosis. In addition, the effects of knockdown on the EMT process, invasion, stemness, and cuproptosis of HNSCC cells were examined by scratch, Transwell, CCK8, sphere formation, and flow cytometry, while changes in related proteins were detected using the immunoblotting method. is highly expressed in most cancers, and it is associated with patient prognosis. expression positively correlates with immunosuppressive cell infiltration and immune checkpoint molecules, while being negatively associated with effector T cells. Moreover, significant correlations are observed between expression and tumor mutation burden (TMB) and microsatellite instability (MSI) in some cancers. In HNSCC, expression is related to advanced clinicopathological factors and unfavorable outcomes. Patients with high expression levels are prone to experience immune escape and benefit less from immune checkpoint inhibitor (ICI) therapy. Moreover, expression may affect EMT, stemness, and cuproptosis resistance outcomes. is an immune-related prognostic biomarker with potential as a prognostic indicator for immunotherapy, and it may also be involved in regulating the EMT process and cuproptosis in HNSCC.